A new study finds that when eating is motivated by pleasure, rewarding chemical signals are created in the brain. In turn, the pleasure response can lead to overeating.
Researchers discovered the phenomenon ultimately affects body mass and may be a factor in the continuing rise of obesity.
“‘Hedonic hunger’ refers to the desire to eat for pleasure, and to enjoy the taste, rather than to restore the body’s energy needs,” said Palmiero Monteleone, M.D., of the University of Naples SUN in Italy and lead author of this study.
“For example, desiring and eating a piece of cake even after a satiating meal is consumption driven by pleasure and not by energy deprivation. The physiological process underlying hedonic eating is not fully understood, but it is likely that endogenous substances regulating reward mechanisms like the hormone ghrelin and chemical compounds such as 2-arachidonoylglycerol (2-AG) are involved.”
In the current study, researchers assessed eight satiated healthy adults, feeding them each their personal favorite food and, later, a less-palatable food of equal caloric and nutrient value.
During the feeding period, researchers periodically measured 2-AG and ghrelin levels. The plasma levels of ghrelin and 2-AG increased during hedonic eating, with the favorite foods, but not with non-hedonic eating.
This increase suggests an activation of the chemical reward system, which overrides the body’s signal that enough has been eaten to restore energy.
“Hedonic hunger may powerfully stimulate overeating in an environment where highly palatable foods are omnipresent, and contribute to the surge in obesity,” said Monteleone.
“Understanding the physiological mechanisms underlying this eating behavior may shed some light on the obesity epidemic. Further research should confirm and extend our results to patients with obesity or with other eating disorders in order to better understand the phenomenon of hedonic eating.”
The study will be published in The Endocrine Society’s Journal of Clinical Endocrinology & Metabolism (JCEM).
Source: The Endocrine Society